Abstract
The 235-1 pituitary tumor clone was utilized to study prolactin secretion after perturbing cyclic AMP and calcium metabolism. Cellular cyclic AMP levels were elevated after treatment with PGE 1, cholera toxin, forskolin, isobutyl-methylxanthine as well as dibutryl cyclic AMP; these cyclic AMP responses were associated with increased prolactinx release. Ionophore A23187 and maitotoxin, which enhance calcium uptake into cells, also amplified prolactin secretion. In contrast, the calmodulin antagonists penfluridol and W7 reduced basal prolactin release. These data support the hypothesis that cyclic AMP, calcium and calmodulin can participate in prolactin release from 235-1 cells.
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